Thomas C. Doetschman, PhD
PhD was in Biophysics and Biochemistry at the University of Connecticut (1980). Postdoctoral trainings were at the Swiss Federal Institute of Technology in Zurich in muscle development, the Friedrich Miescher Institute of the Max Planck Institute in Tubingen Germany in mouse embryology, and the University of Wisconsin in gene targeting under Oliver Smithies. He was Professor of Molecular Genetics at the University of Cincinnati (1988-2005), and subsequently is Professor of Cellular and Molecular Medicine at the University of Arizona. His research in Cincinnati and Tucson has involved the functions of TGFβs and FGFs using knockout mice. He also founded and directed Mouse Genetic Engineering facilities at both institutions.
Cancer Focus
Using mouse genetic engineering he has investigated the role of TGFβ in mouse inflammatory bowel disease and in colon cancer. He determined that the absence of TGFβ signaling leads to autoimmune disease and to increased inflammatory T-cell activity that promotes inflammatory bowel. His recent work on the effect of loss of TGFβ signaling on the role of the gut microbiome in colon cancer suggests that loss of TGFβ, independently of diet, is to increase microbiome polyamine production and to decrease microbiome butyrate production. Both effects are known risk factors for human colorectal cancer. The work indicates that the microbiome may provide risk factors for the development of colon cancer.